The pathogenesis of recurrent ocular chlamydial infections is thought to be immunologically mediated (i.e., hypersensitivity). We have developed an animal model to study the immunological response to chlamydial antigens during infection and challenge. We have chosen to study the immunopathology of guinea pig inclusion conjunctivitis (GPIC), a Chlamydia psittaci strain which produces both ocular and genital infections in guinea pigs. We have clinically, microbiologically, and histologically characterized primary GPIC and a delayed hypersensitivity response to a chlamydial antigen. The delayed hypersensitivity response occurs only in animals previously infected at a mucosal surface by GPIC agent. The chlamydial hypersensitivity antigen has been identified as a polypeptide with an Mr of 57 kD. We have developed, using the guinea pig animal model, a model for corneal opacity and vascularization. Penicillin treatment during primary GPIC arrest the chlamydial developmental cycle at the reticulate body stage and thus prevents development of infectious particles. These reticulate bodies are maintained within inclusions in the host cell and secrete chlamydial antigens which may lead to more severe conjunctivitis and corneal involvement through host immune mechanisms. This may prove a useful model to study complications leading to blindness in trachoma. We are investigating the role of delayed hypersensitivity in salpingitis and tubal infertility using the guinea pig model. Preliminary results indicate following a primary vaginal or oviductal infection, edema and cellular infiltration similar to that seen in a delayed hypersensitivity response occurs in the oviduct upon challenge with the Triton X-100 extract of GPIC. This animal model of chlamydial caused infertility is being further developed.